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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A rise of hemoglobin concentration accompanied by an increase of the total iron in the blood serum of white mice was found under oxygen pressure of 4 atm for an hour (preconvulsive state) and 6 atm (convulsive state). Changes in correlations of hemoglobin fractions in the blood serum were detected in both stages of oxygen poisoning by disc-electrophoresis in 7.5% polyacrylamide gel. A rise of transferrin concentration under these conditions (hyperoxia) was observed. The deflections occurred were less pronounced following administration of urea to the animals before hyperbaric oxygenation.
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PMID:[Hemoglobin, transferrin and total iron content in the blood serum in hyperoxia and during the protective action of urea]. 46 81

The concentration-related viscosity (formula: see text) of DNP-solutions in 4.0 M urea, 0.0005 M tris-buffer (pH 7.5) isolated from cell nuclei of cerebral hemispheres and testicles was determined for mongrel and Wistar rats of 5 groups: I -- normal, II -- after the action of 6 gauge atmospheres of pure oxygen before convulsions beginning, III -- 1 hour, IV -- 4 hours, V -- 12 hours after decompression. It was noted that the concentration-related viscosity of these DNP was equal both for mongrel and inbred rats. No differences in the polymerity degree of brain DNP were detected in all groups of animals under study. The viscosity of testicular DNP was found to decrease by 13.3% 1 hour and 10.3% 4 hours after decompression, whereas 12 hours after it does not differ from the control. Differences in the resistance degree of the brain and testicular DNP to the action of hyperoxia may depend on the cell division rates in these tissues.
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PMID:[Degree of polymerization of rat cerebral hemisphere and testicular DNP-complex during hyperoxia and following it]. 86 17

The rate of lipid peroxidation (by content of the lipid peroxide transformation end product--malonic dialdehyde) in homogenates of rat brain was studied as affected by hyperoxia and with a protective effect of urea in experiments in vivo and in vitro. In both cases an increase is observed in the malonic aldehyde yield with the effect of oxygen under higher pressure. Urea in physiological concentrations lowers the yield under the effect of hyperoxia in vitro. In experiments in vivo introduction of urea also evokes a decrease in the rate of peroxidation. It is established that hyperoxia and urea affect mainly the ascorbate-dependent system of peroxidation. The compositon of phospholipids in the rat brain was studied under the effect of hyperoxia and urea. No changes were found in the number of fractions under the effect of 6at oxygen, only quantitative changes are observed. With introduction of urea before hyperoxia there occurs a normalization in the phospholipid composition. The authors suppose the protective effect of urea to be due to its influence on membranes.
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PMID:[Change in peroxidation and in the phospholipid content in the brain in hyperoxia and the protective action of urea]. 94 11

When breathing with air, pO2 in anesthetized rats was 24.1+/-1.8 mm Hg, while after urea administration it was 19.4+/-1.7 mm Hg. A sharp increase in pO2 was revealed in hyperoxia(911+/-48 mm Hg at 6 atm during first 5 min, and 924+/-38 mm Hg--by the 7th min). The high pO2 was only reduced in 10-15 min after decompression. At a combined action of urea and hyperoxia, pO2 was significantly lower (714+/-52 mm Hg); pO2 in successive cortical layers (0-2400 mcm with a 200-mcm step) was progressively decreasing (from 40.7+/-4.9 mm Hg to 16.0+/-1.0 mm Hg in control, and from 928+/-35 mm Hg to 274+/-64 mm Hg in hyperoxia).
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PMID:[Changes in the oxygen tension of rat cerebral cortex subsequent to hyperoxia and the protective effect of urea]. 95 49

For studying the mechanism of hyperoxia toxic effect on metabolism in the rat brain localization of lysosomes enzymes - acid phosphatase, DNase II and acid peptid-hydrolases were investigated in the brain subcellular fractions under different phases of oxygen poisoning and in the in vitro experiments. Under hyperoxia redistribution of the lysosome enzymes is found between the fraction enriched with lysosomes and the soluble one. The character of redistribution evidences for disturbance of permeability in the brain lysosome membranes under hyperoxia. Urea possessing a protective effect under these conditions prevents from labilization of lysosome enzymes which is evoked by the effect of oxygen hyperoxia. When studying manifestation of the effect of lysosome hydrolases release on the substrate level there were found constancy of DNA content in the brain under hyperoxia and a decrease in polymeric property of the brain DNA an hour after the beginning of the terminal phase of oxygen poisoning.
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PMID:[Lysosome enzymes of brain in hyperoxia and under the effect of urea]. 120 6

Different regimens of oxygenation were studied in rats: acute hypoxia (9,000 m, 3 hrs), acute hyperoxia (0.7 MPa O2), which caused convulsions, and their simultaneous effects. Under these conditions the following parameters were evaluated: the rate of Fe(2+)-induced chemiluminescence, content of nitrogen and peptide catabolism products (urea, urates and middle molecule peptides) as well as total peroxidase activity, content of extraerythrocyte hemoglobin and lactic acid in blood plasma. Distinct inhibition of the chemiluminescence rate was found in all the three experimental groups studied; accumulation of uric acid, middle mass peptides, extraerythrocyte hemoglobin, lactic acid as well as an increase in the total peroxidase activity were observed in hyperoxia and in simultaneous effect of hypo- and hyperoxia; total peroxidase activity was decreased in rats with acute hypoxia. Accumulation of urates and middle mass peptides was considered according to these substances capacity to inhibit free radical oxidation in vivo.
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PMID:[Chemiluminescent analysis and some indicators of nitrogen catabolism in rat blood plasma in hypoxia with subsequent hyperoxia]. 797 75

A 9-year retrospective review of 1,242 admissions to a tertiary burn center identified 137 patients who were intubated and ventilated for a critical airway or pulmonary problem. These patients varied in age from 2 months to 18 years with an average total body surface area (TBSA) burn of 55%. We evaluated this group for evidence of respiratory failure (ARF) as defined by the respiratory failure index (RFI) (PaO2/FIO2 < or = 300). While only 23% of admissions to the burn center were related to flame burns, these injuries accounted for 82% of children who had ARF. Forty-two percent of these intubated children had abnormalities on their admission chest x-ray and 61% of this cohort developed evidence of ARF as defined by the RFI. The development of sepsis along with ARF regardless of TBSA involvement doubles the mortality of ARF alone. Early burn wound excision and grafting is critically important to prevent the late complication of sepsis. We carefully monitor ventilator settings to insure low peak inspiratory pressures, allowing relative hypercapnia and avoiding hyperoxia. Despite an increased number of admissions and critically injured children, we have not seen an increase in morbidity and have had a 53% reduction in mortality in the last 2 years with these techniques. We believe this management offers the best outcome for the pediatric burn victim and would recommend this strategy to other centers dealing with these severely injured children.
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PMID:Mortality and respiratory failure in a pediatric burn population. 826 96

A surface fluorescence method was developed to measure transalveolar transport of water, protons, and solutes in intact perfused lungs. Lungs from c57 mice were removed and perfused via the pulmonary artery (approximately 2 ml/min). The airspace was filled via the trachea with physiological saline containing a membrane-impermeant fluorescent indicator (FITC-dextran or aminonapthalene trisulfonic acid, ANTS). Because fluorescence is detected only near the lung surface due to light absorption by lung tissue, the surface fluorescence signal is directly proportional to indicator concentration. Confocal microscopy confirmed that the fluorescence signal arises from fluorophores in alveoli just beneath the pleural surface. Osmotic water permeability (Pf) was measured from the time course of intraalveolar FITC-dextran fluorescence in response to changes in perfusate osmolality. Transalveolar Pf was 0.017 +/- 0.001 cm/s at 23 degrees C, independent of the solute used to induce osmosis (sucrose, NaCl, urea), independent of osmotic gradient size and direction, weakly temperature dependent (Arrhenius activation energy 5.3 kcal/mol) and inhibited by HgCl2. Pf was not affected by cAMP activation but was decreased by 43% in lung exposed to hyperoxia for 5 d. Diffusional water permeability (Pd) and Pf were measured in the same lung from intraalveolar ANTS fluorescence, which increased by 1.8-fold upon addition of 50% D2O to the perfusate, Pd was 1.3 x 10(-5) cm/s at 23 degrees C. Transalveolar proton transport was measured from FITC-dextran fluorescence upon switching perfusate pH between 7.4 and 5.6; alveolar pH half-equilibrated in 1.9 and 1.0 min without and with HCO3-, respectively. These results indicate high transalveolar water permeability in mouse lung, implicating the involvement of molecular water channels, and establish a quantitative surface fluorescence method to measure water and solute permeabilities in intact lung.
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PMID:Transalveolar osmotic and diffusional water permeability in intact mouse lung measured by a novel surface fluorescence method. 888 57

L-Arginine can be metabolized by nitric oxide (NO) synthase (NOS) to produce NO or by arginase to produce urea and L-ornithine. In the liver, arginase (the AI isoform) is a key enzyme in the urea cycle. In extrahepatic organs including the lung, the function of arginase (the AII isoform) is less clear. Because we found that lung AII was upregulated during 100% O2 exposure in preliminary experiments, we sought to characterize expression of the arginase isoforms and inducible NOS and to assess the functions of arginase in hyperoxic lung injury. Male Sprague-Dawley rats were exposed to 100% O2 for 60 h. Protein expression of AI and AII and their cellular distribution were determined. The activities of arginase and NOS were also measured. Expression of arginase was correlated with that of ornithine decarboxylase, a biochemical marker for tissue repair, in a separate group of rats allowed to recover in room air for 48 h. We found by Western blot analyses that both AI and AII proteins were upregulated after 60 h of hyperoxic exposure (403 and 88% increases by densitometry, respectively) and, like ornithine decarboxylase, remained elevated during the recovery phase. Arginase activity increased by 37%. Immunostaining showed that increases in AI and AII were mainly in the peribronchial and perivascular connective tissues. NOS activity was unchanged and inducible NOS was not induced, but the level of nitrogen oxides in the lung decreased by 67%. Our study showed in vivo induction of arginase isoforms during hyperoxia. The strong expression of arginase in the connective tissues suggests that the function of pulmonary arginase may be linked to connective tissue elements, e.g., fibroblasts, during lung injury and recovery.
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PMID:Induction of arginase isoforms in the lung during hyperoxia. 968 40

Urea levels were measured in the saliva of 30 patients with acute and chronic maxillofacial inflammation treated with multiple modalities including hyperbaric oxygenation (HBO). Urea concentrations were evaluated before, in the course of and after HBO session. A total of four 40-min sessions were made (1 session a day, 1.5 atm). Elevated concentrations of urea after HBO are thought adaptive, serving for elimination of ammonia overproduction in hyperoxia. Urea measurements in the saliva can be used for prediction of oxygen intoxication in the HBO-exposed patients.
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PMID:[The effect of hyperbaric oxygenation on the urea content of the saliva in acute and chronic soft-tissue inflammation in the maxillofacial area]. 995 Dec 97


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